Strong resistance of plants to pathogenic microorganisms is often mediated by disease resistance (R) genes which allow specific molecular recognition of invading organisms (Dangl and Jones, 2001). They trigger a wide variety of defense reactions. In addition, R-independent mechanisms can activate basal defense reactions limiting the extent of infections (Chisholm et al., 2006). Recognition of pathogens by R-dependent or R-independent mechanisms activates partially overlapping defense programs that include coordinated transcriptional re-programming of large sets of genes (Eulgem et al., 2004; Eulgem, 2005). A key signaling molecule mediating R-dependent and R-independent disease resistance is salicylic acid (SA).
Salicylic acid (SA) is signal molecule in the deployment of systemic acquired resistance (SAR). After the initial observation that exogenous application of SA induces resistance in tobacco, SA has been shown to induce resistance in many plant species. Exogenous application of SA also induces expression of the same class of pathogenesis-related (PR) (PR-1, BCL2 (PR-2), and PR-5) genes as those induced during SAR. A strong correlation has been observed between the in vivo increase in SA levels in infected plants and both the expression of PR genes and development of resistance. In addition, SA appears to be involved in the activation of HR cell death and restriction of pathogen spread. The strongest evidence supporting the signaling role of SA in plant defense comes from studies on plants unable to accumulate SA upon pathogen infection. For example, transgenic tobacco and Arabidopsis plants constitutively expressing the Pseudomonas putida nahG gene, which encodes the SA-degrading enzyme salicylate hydroxylase, fail to develop SAR and are hypersusceptible to pathogen infection. Likewise, preventing SA accumulation by application of SA biosynthesis inhibitors also makes otherwise resistant Arabidopsis plants susceptible to Hyaloperonospora parasitica. Conversely, the elevated levels of SA present in the Arabidopsis acd (accelerated cell death; Greenberg et al. 1994; Rate et al. 1999), lsd (lesion simulating disease; Dietrich et al. 1994; Weymann et al. 1995), cpr (constitutive expressor of PR genes; Bowling et al., 1994, 1997; Clarke et al. 1998; Silva et al. 1999), ssi (suppressor of salicylate insensitivity of npr1-5; Shah et al. 1999), and dnd (defense with no HR cell death; Yu et al. 1998) mutants lead to constitutive expression of PR genes and SAR.